However, some malignant cells may develop resistance to anti-NF-κB agents due to genetic modifications affecting different molecules along this pathway in MM cells [33,34], to the central role of NF-κB in increasing the expression of essential regulators of survival (anti-apoptotic molecules and DNA-repair proteins) [35], and also to the assisted supportive effect of the BM-ME, either by soluble factors, exosomes or direct cell contacts [36,37,38]. This evidence concerns the gene NFKB1 and Miyoshi myopathy.